A 26-year-old single male patient who had been graduated from secondary school and had no regular job was admitted to our hospital. Accompanied by his family, the patient voluntarily presented to AMATEM outpatient clinic. On presentation, he complained that he was nervous and short-tempered after he quit using the substance called “bonzai” 2 days ago; he did not sleep at night and became aggressive. His family said that he became very active and talked constantly after quitting the substance 2 days ago; he did not sleep and became aggressive when he was prevented or when his wishes were not met. According to his history, he began to smoke marijuana when he was 12, followed by ecstasy and crack cocaine use several times a month; at the age of 16, he was hospitalized in an addiction clinic, received treatment, and stopped using substance for some time. After about 4 years, he began to use marijuana and ecstasy again with the influence of his friends. He was caught using substance 4 years ago and began to use SCs to prevent detection of drugs in urine drug test, while he was on probation. 6 months ago, he was hospitalized in STRH AMATEM clinic and voluntarily received treatment for 4-5 days, and his serum CK, MB values were normal in tests performed during his hospitalization. He completely stopped using substance after discharge but resumed using SC intensively about 1 week ago. He used crack cocaine once in that period. 2 days ago; he voluntarily stopped using substance completely and presented to our AMATEM outpatient clinic with the existing complaints with the intention of quitting substance. In his psychiatric examination, manic symptoms were prevailing so he was referred to psychiatric ward and admitted for tests and treatment.

In his mental status examination (first examination), he was alert, fully oriented, and cooperative; he was gentle to the interviewer and his attitude was cooperative; his hygiene and grooming were adequate; his mood was elevated; his affect was euphoric and he was irritable; his distractibility and speech content were increased; he was elaborative; his associations were fast; thoughts and attitudes were mild grandiose, but no delusions in thought content or pathology in perception were identified. Psychomotor activity was increased. His insight and judgment were inadequate.

In clinical course and treatment, when he was admitted to the clinic, it was observed that he had expansive mood and irritability, paranoid tendencies (jealousy thoughts related to his girlfriend), and elementary auditory hallucinations (being called out by his name). Upon an increase in his excitation, haloperidol 10 mg and biperiden HCl 2 mg IM were administered, and quetiapine 500 mg/day and risperidone 2 mg/day were added to his treatment. He said he had craving and discomfort so he was given diazepam 5 mg (Table 2).

Other than elevated CK, his hematological and biochemical values were within normal limits. Substance was not detected in urine substance test (Table 2). Despite being restless and irritable in the clinic, he was responsive to suggestions and cooperative. In the next 3 days, he was administered quetiapine 3 × 100 and risperidone 3 mg. He was generally calm and observant of clinical rules.

Beginning of Delirium. In the evening of day 4 of hospitalization, he began to show the following: deterioration of place and time orientation, auditory-visual hallucinations (self-conversation, murmurs, and trying to catch something in the air), delusions (thinking that people around are being changed and saying that he is trapped in a game and nurses are devils and are trying to harm him), disorganized behaviour (random spitting and wandering about), singing songs, trying to get rid of mechanical stabilization, nonsense laughs, and not sleeping. Delirium evaluation scale was applied to the patient as from day 4.

His tests were repeated and his lab results revealed seriously elevated CK and CK-MB values (Table 2, days 3-4). His blood pressure and pulse were normal. Assessment of rigidity and other extrapyramidal system symptoms revealed no finding. Troponin and INR PTZ values requested as a result of consultation of internal diseases department were normal. His treatment was continued with 2000 cc of 5% dextrose and lorezepam mg 2 × 1/2. Despite treatment, his symptoms became severe so he was transferred to AMATEM interim intensive care unit. In his tests were performed on his 1st day in AMATEM, CK: 4267, which was higher than the measurable values, and in addition, CK-MB and MB values were elevated (Table 3, day 5).

His vitals were normal, except mild tachycardia and mild hypertension (max 150/100). His delirium symptoms increasingly continued and lorezepam 9.5 mg/g sublingual, 3000 cc of fluids (1500 isotonic + 1500 5% dextrose), and haloperidol 1 × 5 mg IV were given to the patient. He also developed urinary incontinence. Although there was a mild and temporary improvement in the excitation picture with the existing treatment, the patient was disoriented except for short periods, and his excitation picture continued so in order to provide a complete sedation, he was taken to general ICU (intensive care unit) and continued to be followed. The patient's treatment was continued in intensive care unit with 2.5 mg lorezepam SL 30 mg/g diazepam IV, 3000 cc/g of IV fluids, and 10 mg/g haloperidol IV. The patient calmed down with this treatment and his psychomotor activity and agitation excitation abated. His repeated substance test result was negative for substance. His mental fog and auditory-visual hallucinations continued for another two days. His CK, CK-MB, and MB values began to decrease (Table 2, days 7 and 8). He completely recovered on day 8 of hospitalization and day 3 of his follow-up at ICU. As soon as he regained consciousness, he stated that he wanted to be discharged. He was followed up at outpatient clinic.

It was learned that he began to use SC again 2 days after his discharge. 3 months later, he presented with the intention of quitting SC and had mild hypomanic symptoms at the time. The frequency and quantity of SC use were less than before. He was started on 200 mg carbamazepine, 100 quetiapine, 5 mg olanzapine, and 10 mg diazepam. CK values were normal at baseline and follow-up. No additional clinical pathology suggesting delirium and restlessness, tension, and so forth was observed. He was discharged on day 6 of hospitalization upon his request.

A 30-year-old male, born in Izmit, a high-school graduate, driver, married, was included.

The patient was urgently referred from a psychiatric clinic and voluntarily presented to AMATEM polyclinic accompanied by his father.

His complaint on presentation was “I was using bonzai. I have not used it for 2 days but I drank alcohol but I did not feel relaxed, I want to be admitted to the clinic.” According to the information received from his family, he had not been using substance for 2 days; he was very nervous and did not sleep. The biochemical analysis of the patient revealed that the laboratory levels were high (CK: 1233) so he was admitted for tests and treatment.

According to the story taken from him and his family, he began to smoke marijuana at the age of 12, used drugs including methamphetamine, MDMA, and heroin, and he was jailed for 3 years between the ages of 23 and 26 due to substance use (2009–2012) so he was in mandatory remission but he started to use substance again as soon as he was discharged. He continued to use SC and marijuana on and off for the last 5 years; he has been using SC and marijuana almost every day for the last 1 month but voluntarily stopped using SC and marijuana 2 days ago. After he quit SC, he suffered from tension, contractions, nervousness, nausea, and vomiting and he drank 13 standard drinks once to relieve his complaints, which did not fully abate, and diazepam 10 mg was given intramuscularly twice to the patient at emergency department.

In his mental status examination, he was alert, fully oriented, and cooperative; he was open to communication and partly cooperative with the interview. He made eye contact; memory and intelligence were normal; he was irritable, anxious, and occasionally angry; he had reduced attention and concentration and normal flow of thoughts and connotations; no pathology in thought content and perception; reasoning and insight were preserved; insomnia and psychomotor unrest were present.

Clinical Observation and Treatment. On day 1 of his hospitalization, CK: 1233, CK-MB: 93.1, AST (aspartate aminotransferase) 39, MB: 413, and his substance test revealed THC: 88 nanogram/mL, positive benzodiazepine and ethyl glucuronide (Table 3). Parenteral benzodiazepine (10 mg diazepam in 1500 cc of isotonic), 100 mg quetiapine, and mirtazapine 30 mg were ordered. Sleep was not achieved with these medications and the restlessness of the patient decreased after diazepam administration but increased in general.

On day 2, he had agitation and insomnia with fluctuations in irritability and emotion, and his repeated biochemistry tests revealed CK: 2954, CK-MB: 230, and AST: 74. The patient's treatment was continued with 1500 cc/g isotonic 30 mg/g diazepam IV and 5 mg/g haloperidol IV and 2.5 mg/g lorezepam. After the treatment, the patient's irritability was reduced, and his sleep was regulated. He was alert, cooperative, and oriented. His repeated substance test revealed THC 91 nanogram/mL and the patient tested positive for benzodiazepine and negative for ETG (Table 3). On days 3, 4, 5, 6, and 7, treatment was continued in exactly the same way. His biochemical analyses showed normal results and the patient was observed to be calm and compliant (Table 3). On day 8, oral diazepam 10 mg and lorezepam 2.5 mg were administered. 500 cc isotonic was given. He denied any complaints and was voluntarily discharged.